T cell receptor V beta gene usage in Guillain-Barré syndrome
Autor(es): Khalili-Shirazi A,Gregson N A,Hall M A,Hughes R A,Lanchbury J S
Resumo: We set out to determine whether the T cell receptor (TCR) V beta gene usage in acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is restricted. We separated activated from non-activated peripheral blood T cells with anti-IL2 receptor (anti-CD25) antibody-labelled magnetic beads from four AIDP patients and four normal control (NC) subjects. The TCR V beta gene usage of circulating activated and non-activated T cells was heterogeneous in all the patients and controls, but the activated T cells of all four of the AIDP patients showed a more limited usage of V beta genes and enhanced V beta 15 usage, as compared to the non-activated T cells. This was not seen in the healthy controls. The activated and non-activated T cells from a patient with acute motor and sensory axonal neuropathy (AMSAN) showed a similar V beta gene usage to that of the controls. From a further patient with AIDP, we studied the V beta gene usage of short-term T cell lines reactive to the peripheral nerve myelin proteins P2, P0 and the P0 peptide amino acid sequence 194-208. The V beta gene usage of the lines was heterogeneous, with enhanced usage of V beta 15 in the cell line responsive to the Pzero peptide. We conclude that T cells activated during the immune response associated with AIDP preferentially used V beta 15, which may indicate a restricted response to a common antigen, or a role for an as yet undefined superantigen in the pathogenesis of AIDP.
Palavras-Chave: T cell receptor; V? gene; AIDP; GBS
Imprenta: Journal of the Neurological Sciences, v. 145, n. 2, p. 169-176, 1997
Identificador do objeto digital: 10.1016/S0022-510X(96)00257-2
Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - DNA ; Guillain-Barre Syndrome - Immune response ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - RNA ; Guillain-Barre Syndrome - Immunology
Data de publicação: 1997
